Cats and dogs are the most common companion animals kept by man. As they are both members of the biological order Carnivora, there is a tendency to assume that these two carnivores have similar nutritional requirements. However, there are important differences in the metabolism and nutritional requirements of cats and dogs; see, for example, Morris et al., 1989, in Waltham Symposium 7, Nutrition of the Dog and Cat ed. Burger et al., Cambridge University Press, pp. 35-66.
The Feloidae (Felids, Hyaenids, and Viverrids) diverged from the other members of the order Carnivora relatively early in their evolutionary development. In contrast to the Canoidae (Canids, Ursids, Procyonids and Mustelids), all members of the Feloidae are flesh-eaters, i.e. strict or obligate carnivores. A comparison of the nutritional requirements of cats and dogs as representative members of the Feloidae and Canoidae supports the thesis that specialization consistent with the evolutionary influence of a strict carnivorous diet has occurred in cats; see, for example, MacDonald et al., 1984, Ann. Rev. Nutr. 4, pp. 521-562. A strict carnivorous diet implies the intake of a high protein, moderate fat, and very low carbohydrate diet, following the composition of prey animals. However, omnivorous species, like dogs, are adapted to both plant and animal food sources. Plants, unlike animals, have high carbohydrate stores in the form of starches.
One adaptation to a strictly carnivorous diet are differences in carbohydrate metabolism. For example, while the feline liver contains hexokinase, the enzyme responsible for the first step in glucose metabolism, it contains no glucokinase, which is a hexokinase that exhibits a significantly higher activity for the specific phosphorylation of glucose. Therefore, cats and other obligate carnivores might not be expected to be well adapted for the ingestion of high carbohydrate meals; see, for example, Morris et al., 1989, ibid. Additionally, the release of insulin from a cat's pancreas (insulin causes the cellular uptake of glucose from the blood) is dissimilar to that observed in most other species, appearing to be less responsive to glucose as a stimulus; see, for example, Curry et al., 1982, Comparative Biochemistry and Physiology 72A, pp. 333-338.
Another adaptation to a strictly carnivorous diet relates to the utilization of protein (made up of amino acids) and fat for energy production. Production of glucose from amino acids and fats is called gluconeogenesis. In an omnivore, gluconeogenesis occurs primarily in starvation situations, when the animal needs glucose to fuel its metabolism but can obtain it only from its own muscle protein; see, for example, Zubay, 1993, Biochemistry, Addison-Wesley. However, in an obligate carnivore, such as the cat, gluconeogenesis appears to be active at all times in the liver, regardless of nutritional status. Since an obligate carnivore normally has very low intake of carbohydrate, and its carbon sources are primarily protein and fat, it would be expected that the liver would be adapted for use of proteins as its primary source of glucose, rather than carbohydrate. Additionally, it appears that cats, unlike omnivorous species, have limited ability to regulate the catabolic enzymes of amino acid metabolism. Therefore, when cats are fed a low protein diet, a high obligatory nitrogen loss results. Inability to down-regulate breakdown of amino acids accounts for the observed need for a significantly higher protein intake for cats relative to dogs; see, for example, Rogers et al., 1980, in Nutrition of the Dog and Cat, ed. R. S. Anderson, Oxford-Permagon Press, pp. 145-156.
Furthermore, cats and other obligate carnivores require animal source foods to meet their requirements for certain nutrients. For example, in contrast to dogs, cats cannot convert carotene from plants to Vitamin A; cats cannot synthesize niacin from tryptophan; cats cannot synthesize arachidonic acid from linoleic acid; and cats cannot synthesize sufficient taurine from cysteine. All of these nutrients can be found in a carnivorous diet; see, for example MacDonald et al., 1984, ibid.
Taken together, these data suggest that obligate carnivores, such as cats, are adapted to the use of protein not only for normal structural development and repair, but also as the primary source of energy via the process of gluconeogenesis.
Despite these metabolic differences between a cat, an obligate carnivore, and a dog, a omnivore, cat food formulations have traditionally been very similar to, and frequently derived from, dog food formulations. It has been known that cats have a higher requirement for protein, so cat food formulations have been modified to include higher concentrations of protein compared to dog foods. However, there have been a number of widespread health problems in cats related to such cat food formulations, demonstrating that food developed for dogs is not optimal for cats. For example, cats began developing heart problems relating to lack of taurine in the diet. Taurine is only obtained from animal source protein since vegetable source protein does not contain taurine. Cats also began developing urinary stones, related to too much magnesium in the diet, and hypokalimia, a condition caused by low dietary potassium; see, for example MacDonald et at., 1984, ibid. and Morris et al., 1989, ibid. Pet food companies have responded by supplementing their formulations to correct these problems caused by deficiencies in their cat food formulations. However, these problems demonstrate that there are very basic differences in dietary requirements between the cat, an obligate carnivore, and the dog, an omnivore, and that these differences are not fully addressed in current cat foods.
Commercial cat foods today contain significant, even very high, levels of dietary carbohydrate from corn, wheat and other cereal grains. Dry formulation cat foods, in general, contain higher levels of grain carbohydrates than do canned varieties.
There has been a recent increase in the incidence of feline obesity and feline diabetes in domesticated cats. Twenty percent of adult pet cats are thought to be obese, and feline diabetes is thought to affect one cat out of every four hundred; Panciera et al, 1990, JAVMA 197, pp.1504-1508. Adult-onset diabetes, the most common form in the cat, is almost always insulin dependent and extremely difficult to regulate, even in the face of conscientious care by clinician and owner. The current therapy for feline adult-onset diabetes is administration of insulin. Additionally, for feline obesity, the current therapy is much like that for the treatment of human obesity: it consists of a diet of lower caloric density. Since fat has a higher caloric density than carbohydrate, typically carbohydrate is substituted for fat in order to lower caloric density.
Diabetes mellitus may occur either as a primary disease process or as a secondary complication caused by the destruction of beta cells or insulin resistance due to another disease. In human disease, diabetes is subdivided into type 1 diabetes (insulin dependent, characterized by destruction of the insulin-secreting beta cells of the pancreas) and type 2 diabetes (non-insulin dependent, characterized by insulin resistance). Although there is strong evidence that both types occur in cats, type 2 diabetes appears to be much more frequent, and, in contrast to humans with type 2 diabetes, most cats with type 2 diabetes are insulin dependent; see, for example Lutz et al. 1995, Diabetes Mellitus 25, pp. 527-549.
In type 2 diabetes, insulin secretion and insulin resistance are reduced compared to normal animals. For example, in diabetic cats and humans show markedly reduced or absent insulin secretion during the first phase of insulin response after an increase in glucose, and a markedly delayed and often exaggerated insulin secretion during the second phase of the response. Impaired glucose tolerance is relatively common in cats. Additionally, in cats, marked suppression of insulin secretion may occur within days of a cat showing persistent marked hyperglycemia of approximately 540 milligrams (mg) per deciliter (dL) is present; see, for example Lutz et al., 1995, ibid. This phenomenon is called glucose toxicity. In humans, insulin resistance, i.e. a state in which higher insulin concentrations are required to achieve a given amount of glucose uptake and utilization, is determined genetically; however, in cats a predisposition to insulin resistance has not been demonstrated; see, for example, Rand, 1997, Aust. Vet. Practit. 27, pp. 17-26.
Diabetes in cats is currently difficult to treat and control. Treatment consists of either oral hypoglycemic drugs or insulin therapy. Sulfonylureas are the most common class of oral hypoglycemic drugs. They act by both increasing insulin secretion from beta cells and the sensitivity of peripheral tissues to insulin, therefore, they are only useful if some functional beta cells arc present. Insulin therapy requires careful control and monitoring of blood glucose levels, a challenge to clinician and cat owner. Only 30 to 50% of cats can be managed with oral hypoglycemic drugs. Additionally, approximately 15% of cats with diabetes are transient diabetics, meaning that therapy may be discontinued after several months or weeks; see, for example, Rand, 1997, Aust. Vet. Practit. 27, pp. 68-78.
Current thought on perspectives for treating feline diabetes focuses on understanding the role of the hormone amylin and glucagon-like peptide-1. Amylin receptor antagonists are being developed to treat human type 2 diabetics, and are thought to be potentially useful for cats. Glucagon peptide-1 is also thought potentially useful in treating diabetic cats, Lutz et al., 1995, ibid. There remains, however, a need for a better method to protect cats from diseases of abnormal carbohydrate metabolism, including a method to maintain the well-being of such animals.